[Changes in the balance of biogenic monoamines and their metabolites in the organs of rats with oxygen-induced epilepsy]. / Izmenenie balansa biogennykh monoaminov i ikh metabolitov v organakh krys pri kislorodnoi épilepsii.

The content of some biogenic monoamines and their metabolites in rat brain and heart in different periods of oxygen epilepsia was studied using high performance liquid chromatography with electrochemical detection. It was shown that already at the 5th minute of exposure to oxygen adrenaline, DOPA and some noradrenaline metabolites disappeared in the brain and noradrenaline level reduced. At this period in rat heart the reduction of catecholamine content was the most distinct and serotonin level was unchanged. At the beginning of convulsive period the modifications of biogenic amines content were nonparallel in brain regions: in the heart the reduction of catecholamine level went on, especially in right ventricle. In the terminal phase of oxygen epilepsia brain biogenic amines increased, however, not up to normal meaning, heart catecholamines at this period were at the same level as at the beginning of the convulsive period.

[Kinetics of the oxidative deamination reaction in the preconvulsive period of oxygen-induced epilepsy]. / Kinetika reaktsii okislitel'nogo dezaminirovaniia v dosudorozhnom periode kislorodnoi épilepsii.

Kinetic parameters of monoamine oxidative deamination in compensatory and preconvulsive periods of oxygen epilepsia were studied. It was shown that in rat brain MAO's affinity for serotonin reduced from the 5th minute of exposure to hyperbaric oxygen and went on reducing on the 15th minute. In rat heart the affinity of MAO for serotonin firstly decreased and then returned to normal meaning. Dopamine deamination in rat brain in compensatory period of epilepsia was activated and then was inhibited. In rat heart from the 5th minute of exposure to oxygen dopamine and 2-phenylethylamine deamination was blocked. Tyramine deamination in preconvulsive period of epilepsia changed in a complex manner. It is concluded that the kinetic parameters of monoamine deamination change in the initial phases of exposure to hyperbaric oxygen, and the most distinct modifications take place in rat heart, but not in rat brain.